This project seeks to establish the primary disease lesion in the genetic cardiomyopathy of the Syrian hamster. Early changes in the intracellular electrical activity of the heart cell, in the sarcolemmal calcium handling (including binding and transport) and in the calcium handling ability of other cellular organelles are studied. Techniques employed include: intracellular recording of action potentials, contractility measurements, subcellular fractionation, radioactive calcium binding to membrane fragments, and electron microscopy.